Nishida Haruhiko, Onishi Katsuko, Kurose Satoshi, Tsutsumi Hiromi, Miyauchi Takumi, Takao Nana, Yoshiuchi Sawako, Fujii Aya, Kimura Yutaka
Department of Health Science, Kansai Medical University, Osaka, Japan.
Health Science Center, Kansai Medical University, Osaka, Japan.
Diabetes Metab Syndr Obes. 2020 Jun 23;13:2157-2167. doi: 10.2147/DMSO.S248769. eCollection 2020.
DNA methylation is an epigenetic mechanism that regulates gene expression. The obesity-related () gene is the first gene found to be associated with fat mass and obesity. However, no studies have examined the relationship between weight-loss intervention effect and methylation in obese individuals with whole blood DNA. The purpose of this study was to quantify whole blood DNA methylation and investigate the relationship between body composition, exercise capacity, and blood parameters with a 6-month weight-loss program intervention.
Eighteen female participants (mean age, 50.6 ±12.1 years, body mass index (BMI), 33.5 ± 6.2 kg/m) who completed a 6-month weight-loss program at the obesity outpatient department at the Health Science Center of Kansai Medical University Hospital from March 2017 to October 2018 were included in the analysis. Participants were randomized into a normal treatment group (NTG) and a group with additional resistance training (RTG). Body composition, exercise tolerance and metabolic index were measured in each participant. DNA methylation status in whole blood samples was determined using pyrosequencing. All measurements were taken during the first visit and at the 6-month post-intervention visit.
The methylation rate was significantly decreased in the NTG in CpG1 (p=0.011) and total value of CpG (p=0.011), whereas in the treatment group containing resistance training (RTG), CpG3 (p=0.038) was increased significantly. Furthermore, the independent factors that determine %CpG3 of RTG were visceral fat area change rate (%VFA) (β = -0.568, P = 0.007, R2 = 0.527) and resistance training (β = 0.517, P = 0.012, R2 = 0.527), which have been extracted.
A 6-month weight-loss program, including resistance training, may be associated with decreased visceral fat area changes and increased RTG CpG3 methylation changes. However, further replication studies with larger sample sizes are warranted to verify the findings of this study.
DNA甲基化是一种调节基因表达的表观遗传机制。肥胖相关（）基因是首个被发现与脂肪量和肥胖相关的基因。然而，尚无研究探讨减肥干预效果与肥胖个体全血DNA中该基因甲基化之间的关系。本研究的目的是通过一项为期6个月的减肥计划干预，对全血DNA甲基化进行定量，并研究身体成分、运动能力和血液参数之间的关系。
纳入了18名女性参与者（平均年龄50.6±12.1岁，体重指数（BMI）33.5±6.2kg/m²），她们于2017年3月至2018年10月在关西医科大学医院健康科学中心肥胖门诊完成了一项为期6个月的减肥计划，并纳入分析。参与者被随机分为正常治疗组（NTG）和额外进行阻力训练的组（RTG）。对每位参与者测量身体成分、运动耐量和代谢指标。使用焦磷酸测序法测定全血样本中的DNA甲基化状态。所有测量均在首次就诊时和干预后6个月就诊时进行。
在NTG中，CpG1的甲基化率（p=0.011）和CpG总值（p=0.011）显著降低，而在包含阻力训练的治疗组（RTG）中，CpG3（p=0.038）显著升高。此外，已提取出决定RTG中%CpG3的独立因素为内脏脂肪面积变化率（%VFA）（β = -0.568，P = 0.007，R² = 0.527）和阻力训练（β = 0.517，P = 0.012，R² = 0.527）。
一项为期6个月的包括阻力训练的减肥计划，可能与内脏脂肪面积变化减少和RTG CpG3甲基化变化增加有关。然而，需要进一步进行更大样本量的重复研究来验证本研究的结果。
